Ketoacidosis Management: The Role of Insulin Therapy and Fluid Replacement

Diabetic ketoacidosis (DKA) is a serious metabolic complication primarily seen in individuals with type 1 diabetes, although it can also occur in type 2 diabetes under certain conditions. Effective treatment requires a comprehensive approach, with insulin therapy playing a central role—but only when administered alongside aggressive fluid resuscitation.

The Foundation of DKA Treatment: Fluid Resuscitation

One of the most critical aspects of managing diabetic ketoacidosis is prompt and adequate fluid replacement. Without sufficient hydration, insulin cannot function effectively in lowering blood glucose or halting ketone production. Dehydration in DKA results from osmotic diuresis due to hyperglycemia, leading to significant fluid and electrolyte losses.

The general principle for fluid therapy follows a structured sequence: start with isotonic saline (0.9% sodium chloride), especially in the initial phase. This helps restore intravascular volume, improve tissue perfusion, and support kidney function. After stabilization, the transition may be made to dextrose-containing solutions once blood glucose reaches target levels (typically around 200 mg/dL), preventing hypoglycemia while continuing insulin therapy.

Crystalloids vs. Colloids: What's Preferred?

In clinical practice, crystalloid solutions are favored over colloids for DKA management. Isotonic saline is the first-line fluid because it rapidly expands the extracellular volume and corrects electrolyte imbalances. Colloids, such as albumin, are generally not recommended unless there are specific indications like severe hypoalbuminemia or shock.

Insulin Therapy: Small Doses, Continuous Infusion

Once fluid resuscitation has begun, insulin therapy should be initiated using a low-dose intravenous infusion—typically 0.1 units per kilogram of body weight per hour. This approach steadily reduces blood glucose and suppresses ketogenesis without causing abrupt shifts that could lead to complications like cerebral edema.

Continuous monitoring of blood glucose is essential during treatment. A safe rate of glucose decline is approximately 50–70 mg/dL per hour. Dropping blood sugar too quickly increases the risk of adverse events, particularly in children and young adults.

Potassium Replacement: Don't Overlook Electrolytes

Electrolyte imbalance, especially potassium fluctuations, is common in DKA. Although many patients present with total body potassium depletion, serum levels may initially appear normal or even elevated due to acidosis shifting potassium out of cells. As insulin therapy and fluid correction begin, potassium moves back into cells, risking hypokalemia.

The guiding principle is "insulin with potassium"—meaning potassium supplementation should begin early, provided urine output is confirmed ("see urine, then give potassium"). Monitoring serum potassium every 2–4 hours allows for timely adjustments and prevents life-threatening arrhythmias.

Monitoring and Transitioning to Subcutaneous Insulin

As the patient stabilizes—characterized by normalized pH, resolution of ketonemia, and the ability to eat and drink—transition from IV insulin to subcutaneous insulin can begin. It's crucial to overlap the therapies by at least 30–60 minutes to avoid rebound ketosis.

Throughout the entire treatment process, close observation in an intensive care or monitored setting is advised, especially for high-risk patients. Frequent lab checks, including venous blood gas, electrolytes, glucose, and ketone levels, ensure optimal outcomes.